The aim of this project is to examine the PI component of the auditory evoked potential in an effort to identify the contribution of methodology, medication history, schizophrenia subtype and phenomenology to the presence and nature of PI abnormalities in schizophrenia. Our plan is to examine topographic distributions of PI component (50-70 msec latency following stimulus onset) when different recording and stimulus parameters are used and to identify PI recovery cycle abnormalities in schizophrenia associated with specific topographies. First, changes in the topography of PI as a function of recording protocol (midlatency vs long latency) and stimulus protocol (stimulus trains vs paired stimuli) will be examined in normals. Multivariate analyses will be used to test the hypothesis that the topographic distribution of PI is different when midlatency and long latency protocols are used. Second, we will examine the relationship between PI recovery cycle abnormalities in schizophrenia as assessed by stimulus train and paired stimuli protocols. PI will be examined at sites where its amplitude is maximal in the above studies. To test the hypothesis that abnormalities in PI recovery cycle in schizophrenia,will be found for both stimulus protocols and that abnormalities will be greater at longer interstimulus intervals for paired stimuli protocols and at shorter intervals for stimulus train protocols, we will contrast % recovery measures obtained from normals and patients using each stimulus and recording protocol. Once abnormalities in PI recovery cycle are identified we will examine specific subgroups of schizophrenia to determine whether abnormalities are more prevalent for a particular group. We will also contrast neuroleptic naive and previously. medicated patients to examine whether medication history influences PI abnormalities and examine the relationship between observed abnormalities and phenomenology. Third, we will examine the hypothesis that baseline abnormalities are more prevalent in neuroleptic naive patients than in previously medicated patients and assess whether baseline abnormalities are associated with recovery cycle abnormalities. Our long term goal is to use the information obtained from the proposed studies to develop an auditory evoked potential protocol that is feasible to implement simultaneously with physiologic neuroimaging measures. This will allow a more direct examination of the neural substrates of PI abnormalities in schizophrenia.